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      Stimulation of noradrenergic transmission by reboxetine is beneficial for a mouse model of progressive parkinsonism

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          Abstract

          Parkinson’s disease (PD) is the second most common neurodegenerative disorder and is characterized by motor deficits such as tremor, rigidity and bradykinesia. These symptoms are directly caused by the loss of dopaminergic neurons. However, a wealth of clinical evidence indicates that the dopaminergic system is not the only system affected in PD. Postmortem studies of brains from PD patients have revealed the degeneration of noradrenergic neurons in the locus coeruleus (LC) to the same or even greater extent than that observed in the dopaminergic neurons of substantia nigra (SN) and ventral tegmental area (VTA). Moreover, studies performed on rodent models suggest that enhancement of noradrenergic transmission may attenuate the PD-like phenotype induced by MPTP administration, a neurotoxin-based PD model. The aim of this study was to investigate whether chronic treatment with either of two compounds targeting the noradrenergic system (reboxetine or atipamezole) possess the ability to reduce the progression of a PD-like phenotype in a novel mouse model of progressive dopaminergic neurodegeneration induced by the genetic inhibition of rRNA synthesis in dopaminergic neurons, mimicking a PD-like phenotype. The results showed that reboxetine improved the parkinsonian phenotype associated with delayed progression of SN/VTA dopaminergic neurodegeneration and higher dopamine content in the striatum. Moreover, the alpha1-adrenergic agonist phenylephrine enhanced survival of TH+ neurons in primary cell cultures, supporting the putative neuroprotective effects of noradrenergic stimulation. Our results provide new insights regarding the possible influence of the noradrenergic system on dopaminergic neuron survival and strongly support the hypothesis regarding the neuroprotective role of noradrenaline.

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          Stages in the development of Parkinson's disease-related pathology.

          Heiko Braak, Estifanos Ghebremedhin, Udo Rüb … (2004)
          The synucleinopathy, idiopathic Parkinson's disease, is a multisystem disorder that involves only a few predisposed nerve cell types in specific regions of the human nervous system. The intracerebral formation of abnormal proteinaceous Lewy bodies and Lewy neurites begins at defined induction sites and advances in a topographically predictable sequence. As the disease progresses, components of the autonomic, limbic, and somatomotor systems become particularly badly damaged. During presymptomatic stages 1-2, inclusion body pathology is confined to the medulla oblongata/pontine tegmentum and olfactory bulb/anterior olfactory nucleus. In stages 3-4, the substantia nigra and other nuclear grays of the midbrain and forebrain become the focus of initially slight and, then, severe pathological changes. At this point, most individuals probably cross the threshold to the symptomatic phase of the illness. In the end-stages 5-6, the process enters the mature neocortex, and the disease manifests itself in all of its clinical dimensions.
          Article 0 comments Cited 660 times – based on 0 reviews     Review now
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            The tail suspension test as a model for assessing antidepressant activity: review of pharmacological and genetic studies in mice.

            John F. Cryan, Cedric Mombereau, Annick Vassout (2005)
            Since its introduction almost 20 years ago, the tail suspension test has become one of the most widely used models for assessing antidepressant-like activity in mice. The test is based on the fact that animals subjected to the short-term, inescapable stress of being suspended by their tail, will develop an immobile posture. Various antidepressant medications reverse the immobility and promote the occurrence of escape-related behaviour. This review focuses on the utility this test as part of a research program aimed at understanding the mechanism of action of antidepressants. We discuss the inherent difficulties in modeling depression in rodents. We describe how the tail suspension differs from the closely related forced swim test. Further, we address some key issues associated with using the TST as a model of antidepressant action. We discuss issues regarding whether it satisfies criteria to be a valid model for assessing depression-related behavioural traits. We elaborate on the tests' ease of use, strain differences observed in the test and gender effects in the test. We focus on the utility of the test for genetic analysis. Furthermore, we discuss the concept of whether immobility maybe a behavioural trait relevant to depression. All of the available pharmacological data using the test in genetically modified mice is collated. Special attention is given to selective breeding programs such as the Rouen 'depressed' mice which have been bred for high and low immobility in the tail suspension test. We provide an extensive pooling of the pharmacological studies published to date using the test. Finally, we provide novel pharmacological validation of an automated system (Bioseb) for assessing immobility. Taken together, we conclude that the tail suspension test is a useful test for assessing the behavioural effects of antidepressant compounds and other pharmacological and genetic manipulations relevant to depression.
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              Norepinephrine deficiency in Parkinson's disease: the case for noradrenergic enhancement.

              Alberto Espay, Peter LeWitt, Horacio Kaufmann (2014)
              The dramatic response of most motor and some nonmotor symptoms to dopaminergic therapies has contributed to maintaining the long-established identity of Parkinson's disease (PD) as primarily a nigrostriatal dopamine (DA) deficiency syndrome. However, DA neurotransmission may be neither the first nor the major neurotransmitter casualty in the neurodegenerative sequence of PD. Growing evidence supports earlier norepinephrine (NE) deficiency resulting from selective degeneration of neurons of the locus coeruleus and sympathetic ganglia. Dopaminergic replacement therapy therefore would seem to neglect some of the motor, behavioral, cognitive, and autonomic impairments that are directly or indirectly associated with the marked deficiency of NE in the brain and elsewhere. Therapeutic strategies to enhance NE neurotransmission have undergone only limited pharmacological testing. Currently, these approaches include selective NE reuptake inhibition, presynaptic α2 -adrenergic receptor blockade, and an NE prodrug, the artificial amino acid L-threo-3,4-dihydroxyphenylserine. In addition to reducing the consequences of deficient noradrenergic signaling, enhancement strate gies have the potential for augmenting the effects of dopaminergic therapies in PD. Furthermore, early recognition of the various clinical manifestations associated with NE deficiency, which may precede development of motor symptoms, could provide a window of opportunity for neuroprotective interventions.
              Article 0 comments Cited 80 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Grzegorz Kreiner: kreiner@if-pan.krakow.pl
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 27 March 2019
                Publication date PMC-release: 27 March 2019
                Publication date Collection: 2019
                Volume: 9
                Electronic Location Identifier: 5262
                Affiliations
                [1 ]ISNI 0000 0001 1958 0162, GRID grid.413454.3, Department Brain Biochemistry, Institute of Pharmacology, , Polish Academy of Sciences, ; 31-343 Kraków, Smętna 12, Poland
                [2 ]ISNI 0000 0001 2227 8271, GRID grid.418903.7, Department Pharmacokinetics and Drug Metabolism, , Institute of Pharmacology, Polish Academy of Sciences, ; 31-343 Kraków, Smętna 12, Poland
                [3 ]ISNI 0000 0004 1936 9748, GRID grid.6582.9, Institute of Applied Physiology, , University of Ulm, ; 89081 Ulm, Germany
                [4 ]ISNI 0000 0001 2190 4373, GRID grid.7700.0, Institute of Anatomy and Cell Biology, , University of Heidelberg, ; 69120 Heidelberg, Germany
                Author information
                http://orcid.org/0000-0001-9622-3476
                Article
                Publisher ID: 41756
                DOI: 10.1038/s41598-019-41756-3
                PMC ID: 6437187
                PubMed ID: 30918302
                SO-VID: 42fb83bf-13ff-4b7d-8933-e4a7668eebae
                Copyright © © The Author(s) 2019
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 8 November 2018
                Date accepted : 14 March 2019
                Funding
                Funded by: Supported by grants no 2011/03/B/NZ7/05949 (Opus2) and 2017/25/B/NZ7/02406 (Opus13) from the National Science Center.
                Funded by: Supported by statutory funds from the Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
                Funded by: Supported by grants no 2011/03/B/NZ7/05949 (Opus2).
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2019

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